Ischemic tolerance of the brain from bench to bedside

Neurons can be preconditioned by various procedures to resist ischemic events. The preconditioning mechanism induced is characterized by a brief episode of ischemia that renders the brain more resistant against subsequent longer ischemic events. This ischemic tolerance has been shown in experimental animal model of cerebral ischemia and recently in humans. In contrary to the heart, the basic molecular mechanisms of cerebral ischemic tolerance are largely unknown in detail, but is initiated over several hours or days, and can persists for up to a week or more. The pathophysiological course can be divided in (i) induction, (ii) transduction and (iii) tolerance. The cellular mechanism is explained leading to the synthesis of stress proteins. These proteins works as cellular „chaperons" by unfolding misfolded cellular proteins and helping the cell to dispose of unneeded denatured proteins. Implications to clinical and therapeutic implications are drawn